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. 2007 Aug 3;8(9):858–863. doi: 10.1038/sj.embor.7401045

Figure 4.

Figure 4

Rtf1 cooperates with the Paf1 complex during somitogenesis. (A,B) Knockdown of ctr9 results in defects that are similar to but weaker than those of kt641 mutants. Embryos injected with ctr9 MO1 (A), but not 5-mismatched MO1 (B), show reduced pigmentation, abnormal cardiogenesis (arrow), small ears (arrowhead), slightly shortened tails and disorganized somite boundaries in the tail (square bracket) at 36 h post-fertilization. Two independent ctr9 MOs cause similar morphological defects. (B) 5-mispaired ctr9 MO1 hardly impairs development. (C–E) At the 12-somite stage, no marked defects were observed in ctr9 MO-injected embryos (C). 5-mispaired control MO1 had no effect on the kt641 phenotype (D), whereas injection of ctr9 MO1 into kt641 mutant embryos resulted in an enhanced segmentation defect with few segmentation boundaries (E). The square brackets in (D) and (E) indicate the posterior somites with obscure boundaries. (F) Number of segmented somites in ctr9 MO1-injected wild-type embryos (n=82), ctr9 5-mismatched MO1-injected kt641 mutants (n=18) and ctr9 MO1-injected kt641 mutants (n=23) at 24 h post-fertilization. Error bars represent the s.d. P<0.001 between single mutants (kt641<5-mismatched MO1 or wt<ctr9 MO1) and double mutants (kt641<ctr9 MO1) are represented. (G–J) her1 expression in 5-mismatched control MO1-injected (G,I), ctr9 MO1-injected (H,J) wild-type (G,H) or kt641 mutant (I,J) embryos. In comparison with wild-type siblings injected with 5-mismatched control MO1 (G), those injected with the ctr9 MO1 show reduced her1 expression (H). This reduction is enhanced in kt641 mutant embryos injected with ctr9 MO1 (J). MO, morpholino oligonucleotides.